- Intestinal microbiota - characteristics
- Intestinal microbiota - composition in different periods of life
- Intestinal microbiota - impact on the body
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The intestinal microbiota is all the microorganisms that live in the large intestine. Among them, the best recognized are bacteria, of which there are over 1000 species in a he althy person. The composition and abundance of microbiota are closely related to he alth, mood and brain function. Find out how gut bacteria affect your body.
Microbiotais a group of microorganisms of various kinds that live in the host organism and on its surface.Microbiome means the same as microbiota . Both terms are used interchangeably. However, the term "microflora" is abandoned, which suggests that the microorganisms in the host's body are of plant origin.
The human microbiota includes not only bacteria, but also viruses, archaea and eukaryotic organisms. However, the diversity and role of bacteria has been best studied. Bacteria living in the human body have been identified thanks to gene sequencing. These discoveries made it possible to understand the relationship between the microbiome and the host.
Intestinal microbiota - characteristics
The gut microbiome is one of the elements of the whole organism's microbiome, which is of great importance for the homeostasis of the human body.
The intestinal bacteria are those found in the large intestine.A he althy adult human typically harboring more than 1,000 species of bacteriabelonging to relatively few known types of bacteria. Anaerobic bacteria of the Bacteroidetes and Firmicutes types are predominant.
Variability of the gut microbiota
The gut microbiota is variable - it is not the same both in different people and in the same person at different times. The differences between individuals are very clear.
It is known that the overall diversity of the human gut microbiota changes throughout life. It continues to increase from birth to around age 12, remaining relatively stable throughout adulthood and then decreasing in later years.
One study found that around 70% of the microbiota remains unchanged in a year without antibiotic treatment. Observations have shown that some species are likely to be stable over decades, if not for the lifetime of an individual, as evidenced by the identification of the same bacterial species among family members but not between individualsunrelated.
Thus, some bacteria remain the same in he althy people, and some change throughout their lives. External factors also change the microbiome over time. These include, among others :
- infections,
- medications taken,
- lifestyle
- and diet changes.
LifeLines Deep study using bacterial genome sequencing on more than 1,000 people found diet to be a major modulator of gut microbiome variability.
Reasons for reducing the diversity of the gut microbiota
The gut microbiome is very rich compared to other parts of the body. A large diversity of the intestinal microbiota is a feature of he althy people. Disease states lead to its impoverishment in terms of species diversity.
Less bacterial diversity was observed in people with:
- inflammatory bowel disease,
- psoriatic arthritis,
- type 1 diabetes,
- atopy,
- celiac,
- obesity,
- with type 2 diabetes
- and arterial stiffness compared to he althy people.
The link between reduced diversity and disease indicates that the species-rich gut ecosystem is more resistant to environmental influences.
Main types of gut bacteria
Diversity is considered a good indicator of a "he althy gut". The main types of gut bacteria in terms of abundance are:
- Firmicutes,
- Bacteroidetes,
- Actinobacteria,
- Proteobacteria,
- Verrucomicrobia
- and Fusobacteria.
The composition of the gut microbiome naturally changes with age. It depends mainly on the diet.
Both 2-3-year-olds and adults are dominated by the same bacteria, which is due to the fact that children around the age of 3 already eat exactly the same food as adults.
Intestinal microbiota - composition in different periods of life
| Life span | Dominant intestinal bacteria |
| Moment of birth | Enterococcus, Staphylococcus |
| First month of life | Bifidobacteriaceae |
| Sixth month of life | Clostridiacea, Ruminococcaceae, Lachnnospraceae |
| First year of life | Bacteriodes, Clostridium, Ruminococcum |
| Second - third year of life | Firmicutes, Bacteroidetes |
| Adulthood | Firmicutes, Bacteroidetes |
Intestinal microbiota - impact on the body
The gut microbiota affectsthe body's physiology in many aspects. Classically, its role is seen mainly in the digestion of nutrients that are indigestible to enzymes in the digestive system. However, this is only the tip of the iceberg. Changes in the composition of the microbiome (dysbiosis) occur in many diseases.
It is often unclear, however, whether it is altered microbiota that causes disease or whether the disease affects the composition of gut bacteria. What is the importance of gut bacteria for the body?
Microbiota and the gut-brain axis
You can often hear the saying that the gut is our second brain. It is absolutely justified. In the body, two-way signaling takes place between the gut microbiota, the gut and the brain. It takes place via the neural pathways that include the central and intestinal nervous systems and the circulatory system.
Signaling by the circulatory system involves:
- axis hypothalamus - pituitary - adrenal glands,
- immune system regulators,
- hormones,
- neurotransmitters
- and bacterial metabolites such as short chain fatty acids.
Preclinical studies have shown the influence of the intestinal microflora on:
- nociceptive reflexes (reflexes in response to tissue-damaging stimuli),
- food intake,
- emotional and social behavior,
- stress response
- and the neurochemistry of the brain.
In studies on mice, it has been shown that microbiota is necessary for the social development of mice and is involved in neurodevelopmental disorders, including autism spectrum disorders.
Mice lacking gut microbiota have been shown to have an exaggerated stress response compared to control animals. These mice also show increased motor activity and less severe anxiety behavior compared to control mice.
In contrast, the administration of the probiotic L. rhamnosus (JB-1) to mice decreased the levels of corticosterone secreted under stress and anxiety-related behaviors.
These data strongly emphasize the importance of the microbiome-gut-brain axis for normal neurological development and function.
Why does the microbiome affect the brain?
The gut microbiome produces short-chain fatty acids that affect the integrity of the blood-brain barrier by increasing the production of tight junction proteins - claudin-5 and occludin.
Tight connections are connections between two cells of the body (in this case, the intestinal epithelium) that close the space between these cells, making the cells very tight to each otherattached.
These proteins are arranged in strips to form a branched network. They must appear on the surface of both adjacent cells to be able to connect with each other.
The existence of properly functioning tight connections between the intestinal epithelial cells, and thus the increased integrity of the blood-brain barrier, limits the penetration of undesirable metabolites between the cells into the extracellular space.
When the integrity of epithelial cells is impaired, harmful substances from the intercellular fluid enter the blood and then the brain. This phenomenon adversely affects brain function, cognition and mood.
Influence of the microbiome on the psyche
Research provides evidence thatgut microbiota can modulate the stress response and also contribute to anxiety, depression and cognition.
Numerous placebo-controlled studies show that ingestion of probiotic bacteria causes significant changes in brain activity as assessed by functional magnetic resonance imaging, concentration, emotion and sensation processing.
A number of experiments have shown a beneficial effect of taking probiotics on the mood of people with psychological problems, a tendency to sadness and bad thoughts, anxiety and depression.
Many people with alcohol dependence show changes in gut permeability and the gut microbiome. Increased intestinal permeability in these people was significantly associated with higher scores for depression, anxiety and craving after 3 weeks of abstinence.
Intestinal microbiota and digestion
The gut microbiota is an integral part of the host's digestion and nutrition and can produce nutrients from substrates otherwise indigestible by the host.
Gut bacteria break down fiber, some proteins, saccharides, and polyphenols. The microbes release short chain fatty acids from digestive indigestible fiber, which is an important source of energy for the intestinal mucosa and is crucial for modulating the immune response and the formation of tumors in the gut.
Intestinal microbiota and immunity
The interactions between the microbiota and the host's immune system are numerous and complex. The role of the immune system is to learn to recognize commensal ("good") and pathogenic (pathogenic) bacteria.
In turn, microbiota is an integral part of educating the immune system to function properly.
Microbiota influences immune homeostasis inside and outside the gut. Participates, inter alia, in the differentiation of system regulatory T cellsimmune. These mechanisms are of great importance for the pathogenesis and treatment of inflammatory diseases.
Role of commensal bacteria
Commensal bacteria and probiotics may promote the integrity of intestinal barriers. Thanks to this, pathogenic bacteria and their metabolites have a much lower chance of penetrating the circulatory system.
Commensal bacteria contribute to the strengthening of immunity at the gut level mainly by preventing the invasion of pathogenic bacteria and supporting the development of the host's immune system.
Good gut bacteria hinder the colonization of pathogenic bacteria by competing with them for nutrients and attachment sites on the surface of the colon mucosa.
Commensal bacteria also prevent the invasion of pathogenic bacteria by lowering the intestinal pH through the production of lactate and short-chain fatty acids (SCFA). Another way is to produce metabolites that inhibit growth or kill potentially pathogenic bacteria.
Although the mechanisms by which the microbiome interacts with the immune system are not thoroughly investigated, it is known with certainty that a he althy microbiome positively influences immunity both as a biological barrier and by shaping acquired immunity.
Intestinal microbiota and obesity
The gut microbiota may play a role in the development of obesity. Most studies of overweight and obese people show dysbiosis, which is characterized by less diversity in the microbiome. An example may be the research carried out:
- Mice with an uninhabited digestive tract that are transplanted with fecal microbes from obese humans gain more weight than mice that receive microbes from he althy humans.
- A large study of twins in the UK found that a type of Christensenella was rare in overweight people and that when administered to mice free of their own microbiota, it prevented weight gain. The presence of Christensenella in the gastrointestinal tract, as well as Akkermansia, has been associated with lower accumulation of fat in the internal organs of the abdominal cavity.
Most of the evidence supporting the thesis about the role of microbiota in obesity comes from studies in mice. However, it is also observed that weight gain in humans over 10 years is associated with low microbiota diversity, and this relationship is worsened by low dietary fiber consumption.
Dysbiosis of the gut microbiota likely promotes diet-induced obesity and metabolic complications through a variety of mechanisms, including:
- immunity dysregulation,
- changed energy regulation,
- altered gut hormone regulation
- and pro-inflammatory mechanisms caused by lipopolysaccharide endotoxins, crossing the intestinal barrier and entering the portal circulation.
Increasing fatty acid oxidation and energy expenditure as well as reducing fatty acid synthesis reduces the tendency to obesity.
Akkermansia muciniphila, Bacteroides acidifaciens, Lactobacillus gasseri and short-chain fatty acids have been found to increase fatty acid oxidation in adipose tissue.
Other microbiome mechanisms favoring weight control are:
- adipocyte differentiation,
- increasing muscle thermogenesis,
- enhancing the expression of genes related to fatty acid oxidation,
- silencing the expression of genes responsible for the synthesis of fat in the body.
The literature summarizes that an imbalance in the gut microbiota and the lack of certain types of bacteria promote greater weight gain with the same diet.
Intestinal microbiota and colorectal cancer
Research has shown that the gut microbiota can influence the risk and progression of colorectal cancer by modulating mechanisms such as inflammation and DNA damage, and by producing metabolites involved in tumor progression or suppression.
Dysbiosis of the gut microbiota has been observed in patients with colorectal cancer, with a reduction in the number of commensal bacteria species (butyrate-producing bacteria) and an enrichment of harmful bacterial populations (pro-inflammatory opportunistic pathogens).
Colorectal cancer is characterized by altered production of bacterial metabolites directly involved in the metabolism of cancer cells, including short-chain fatty acids and polyamines. Emerging evidence suggests that diet has a significant influence on the risk of developing this cancer.
Consumption of high-fiber foods and dietary supplementation with polyunsaturated fatty acids, polyphenols, and probiotics known to regulate the gut microbiota may not only be a potential mechanism for reducing the risk of colorectal cancer.
It may also enhance the response to cancer therapy when used in addition to conventional treatment of colorectal cancer.
Intestinal microbiota and intestinal diseases
Gut dysbiosis and decreased microbiome diversity are regularly found in people with inflammatory bowel disease.The depletion of the microbiota in some bacteria and the loss of their protective functions may have a significant impact on the course of the disease.
Many of the bacterial protective functions associated with IBD are due to their ability to ferment dietary fiber and produce short-chain fatty acids.
Intestinal inflammation reduces the number of species of commensal bacteria and creates conditions for the growth of pathogenic bacteria. These, in turn, are capable of increasing the multiplication and worsening of the condition of the sick.
Pathogenic bacteria that potentially play the greatest role in IBD are:
- Escherichia and Shigella,
- as well as Fusobacterium species.
Large changes in the microbiome are observed in patients, both in terms of the number of species and their proportion to each other.
Intestinal microbiota and the circulatory system
The microbiome can have both positive and negative effects on cardiovascular he alth. The beneficial effect is related to the regulation of the lipid profile - increasing the level of "good" HDL cholesterol and lowering the level of triglycerides in the blood. Taking probiotics, mainly Lactobacilli, is known to help lower cholesterol levels.
On the other hand, bacterial dysbiosis and an excess of pathogenic bacteria lead to the production of trimethylamine N-oxide (TMAO), which promotes the formation of atherosclerotic plaque in blood vessels and can lead to heart attacks and strokes.
TMAO is produced by the metabolism of choline and L-carnitine, which are typical components of a diet containing animal protein and play important functions in the body. It is not known exactly what components of the microbiome are responsible for the increased production of TMAO and the increased risk of heart disease.
Some sources postulate that it could be:
- Cytomegalovirus,
- Helicobacter,
- Chlamydia
- and C. pneumoniae.
Studies have shown that in people with a significantly higher proportion of Prevotella bacteria in the microbiome, there was a problem with elevated TMAO levels. At the same time, the concentration of this oxide was normal in people with a high percentage of Bacteroides.
Intestinal microbiota and diabetes
Scientific research confirms the role of the gut microbiome in metabolic diseases, including type 2 diabetes.
It is clear from animal studies that the microbiome is involved in the metabolism of glucose. Based on 42 observational studies on humans, bacteria have been proposed whose presence in the microbiome promotes the occurrence of type 2 diabetes.
These are bacteria of the following types:
- Ruminococcus,
- Fusobacterium
- and Blautia.
The types of bacteria that reduce the likelihood of type 2 diabetes are:
- Bifidobacterium,
- Bacteroides,
- Faecalibacterium,
- Akkermansia
- and Roseburia.
Lactobacillus also belongs to the bacteria beneficial in diabetes, but the results of research regarding them are not so clear.
Type 2 diabetes is associated with elevated levels of inflammatory cytokines, chemokines, and inflammatory proteins. While some gut microbes and their metabolites promote low-grade inflammation, others stimulate anti-inflammatory cytokines and chemokines.
Bacteria associated with a lower risk of type 2 diabetes may contribute to increased expression of anti-inflammatory cytokines that protect against insulin resistance and restore insulin sensitivity.
Other features associated with type 2 diabetes are low-grade inflammation and increased intestinal permeability. It has been shown that the indicated intestinal bacteria reduce the production of pro-inflammatory compounds and strengthen tight connections between intestinal epithelial cells. In this way, they reduce the risk of developing type 2 diabetes.
The gut microbiota is associated with type 2 diabetes through its effects on glucose homeostasis and insulin resistance in major metabolic organs, such as:
- liver,
- muscles
- and fat.
Microbiota and its products can modulate intestinal hormones and enzymes, and reduce insulin resistance and improve glucose tolerance.
Intestinal bacteria considered beneficial in the prevention of type 2 diabetes may, among others :
- increase glycogen synthesis and decrease the expression of genes related to gluconeogenesis in the liver,
- improve glucose transporter-4 (GLUT4) translocation and insulin-stimulated glucose uptake,
- increase the expression of GLUT-4 in the muscles, which may have anti-diabetic effects,
- reduce the expression of hepatic flavin monooxygenase 3 (Fmo3), a key enzyme in xenobiotic metabolism, the reduced secretion of which prevents the development of hyperglycemia and hyperlipidemia in insulin-resistant mice,
- regulate the expression of genes associated with hyperglycemia,
- increase adiponectin levels in fat, thus improving insulin sensitivity.
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